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Human brain imaging studies have revealed several regions that are activated in patients with chronic pain. In rodent brains, functional changes due to chronic pain have not been fully elucidated, as brain imaging techniques such as functional magnetic resonance imaging and positron emission tomography (PET) require the use of anesthesia to suppress movement. Consequently, conclusions derived from existing imaging studies in rodents may not accurately reflect brain activity under awake conditions. In this study, we used quantitative activation-induced manganese-enhanced magnetic resonance imaging to directly capture the previous brain activity of awake mice. We also observed and quantified the brain activity of the spared nerve injury (SNI) neuropathic pain model during awake conditions. SNI-operated mice exhibited a robust decrease of mechanical nociceptive threshold 14 days after nerve injury. Imaging on SNI-operated mice revealed increased neural activity in the limbic system and secondary somatosensory, sensory-motor, piriform, and insular cortex. We present the first study demonstrating a direct measurement of awake neural activity in a neuropathic pain mouse model.

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In this chapter, we provide an overview of neuroimaging studies in chronic pain. We start with an introduction about the phenomenology of pain. In the following section, the application of functional and structural imaging techniques is shown in selected chronic pain syndromes (chronic back pain, fibromyalgia syndrome (FMS), phantom limb pain, and complex regional pain syndrome (CRPS)), and commonalities and peculiarities of imaging correlates across different types of chronic pain are discussed. We conclude this chapter with implications for treatments, with focus on behavioral interventions, sensory and motor trainings, and mirror and motor imagery trainings.

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BACKGROUND: This study aims to assess the impact of ultrasound diagnosis in patients with chronic pelvic pain (CPP). METHODS: We will carry out a comprehensive electronic search from the databases below: PUBMED, EMBASE, Cochrane Library, PSYCINFO, Web of Science, Cumulative Index to Nursing and Allied Health Literature, Allied and Complementary Medicine Database, Chinese Biomedical Literature Database, China National Knowledge Infrastructure, and WANGFANG databases from inception to July 1, 2019. The case-controlled studies focusing on impact of ultrasound diagnosis for patients CPP will be included in this study. Two authors will independently conduct all study selection, data collection, and risk of bias assessment. The risk of bias assessment will be assessed using Quality Assessment of Diagnostic Accuracy Studies tool. We will apply RevMan V.5.3 software and Stata V.12.0 software for data pooling and statistical analysis. RESULTS: This study will present pooled effect estimates regarding the impact of ultrasound diagnosis for CPP by assessing sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio of ultrasound to determine the diagnostic accuracy of ultrasound diagnosis for CPP. CONCLUSION: This study will provide modest evidence for the diagnostic accuracy of ultrasound in patients with CPP. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42019142799.

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Comorbid depressive symptoms (CDS) in chronic pain are a common health problem, but the neural circuit mechanisms underlying these symptoms remain unclear. Here we identify a novel pathway involving 5-hydroxytryptamine (5-HT) projections from the dorsal raphe nucleus (5-HTDRN) to somatostatin (SOM)-expressing and non-SOM interneurons in the central nucleus of the amygdala (CeA). The SOMCeA neurons project directly to the lateral habenula, an area known involved in depression. Inhibition of the 5-HTDRNâSOMCeA pathway produced depression-like behavior in a male mouse model of chronic pain. Activation of this pathway using pharmacological or optogenetic approaches reduced depression-like behavior in these mice. Human functional magnetic resonance imaging data showed that compared to healthy controls, functional connectivity between the CeA-containing centromedial amygdala and the DRN was reduced in patients with CDS but not in patients in chronic pain without depression. These findings indicate that a novel 5-HTDRNâSOMCeAâlateral habenula pathway may mediate at least some aspects of CDS.

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HISTORY: A 68-year-old woman presented with chronic back pain, a poor general condition, weight loss of 20âkg in the last 6 months and paretic hands. FINDINGS AND DIAGNOSIS: The patient had pareses of hand- and finger muscles on both sides with corresponding deficits proven by EMG. MRI revealed an intraspinal mass affecting the cervical and thoracic spine with myelon compression. Histologically IgG4-positive plasma cells were detected and IgG4-RD with spinal pseudotumor and resulting cervicothoracic myelopathy were diagnosed. THERAPY AND COURSE: After initiation of high-dose glucocorticoid therapy (100âmg i.âv. over 7 days with reduction afterwards) and cyclophosphamide-pulse-therapy (initially 750âmg i.âv., cumulative dose of 4500âmg in 6 months), the general condition and motor deficits improved. CONCLUSIONS: The CNS are a rare manifestation of IgG4-RD. The tumor typically grows displacing, is best visualized on MRI or PET-CT, presenting clinically the corresponding pain and neurological deficits and shows characteristic histology. Steroids and, as in our case helpful, advanced immunosuppression can be a promising treatment option.

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Pain is a highly complex and individualized experience with biopsychosocial components. Neuroimaging research has shown evidence of the involvement of the central nervous system in the development and maintenance of chronic pain conditions, including urological chronic pelvic pain syndrome (UCPPS). Furthermore, a history of early adverse life events (EALs) has been shown to adversely impact symptoms throughout childhood and into adulthood. However, to date, the role of EAL's in the central processes of chronic pain have not been adequately investigated. We studied 85 patients (56 females) with UCPPS along with 86 healthy controls (HCs) who had resting-state magnetic resonance imaging scans (59 females), and data on EALs as a part of the Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network Study. We used graph theory methods in order to investigate the impact of EALs on measures of centrality, which characterize information flow, communication, influence, and integration in a priori selected regions of interest. Patients with UCPPS exhibited lower centrality in the right anterior insula compared to HCs, a key node in the salience network. Males with UCPPS exhibited lower centrality in the right anterior insula compared the HC males. Females with UCPPS exhibited greater centrality in the right caudate nucleus and left angular gyrus compared to HC females. Males with UCPPS exhibited lower centrality in the left posterior cingulate, angular gyrus, middle temporal gyrus, and superior temporal sulcus, but greater centrality in the precuneus and anterior mid-cingulate cortex (aMCC) compared to females with UCPPS. Higher reports of EALs was associated with greater centrality in the left precuneus and left aMCC in females with UCPPS. This study provides evidence for disease and sex-related alterations in the default mode, salience, and basal ganglia networks in patients with UCPPS, which are moderated by EALs, and associated with clinical symptoms and quality of life (QoL).

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Chronic pain affects 50% of adults with sickle cell disease (SCD). Although central sensitization is thought to contribute to the pathogenesis of this chronic pain, no studies have examined differences in functional connectivity of the brain between patients with SCD with and without chronic pain. We performed an observational cohort study using resting-state functional MRI (rsfMRI) of the brain on adults with SCD with and without chronic pain. We tested the hypothesis that, compared to those without chronic pain, those with chronic pain would have differences in functional connectivity between the periaqueductal grey (PAG) and other regions of the brain. Twenty-two adults with SCD, 15 with chronic pain and 7 without chronic pain, as well as 10 African-American controls, underwent rsfMRI of the brain. When SCD patients with chronic pain were compared to those without chronic pain, significant differences in connectivity were noted between the PAG and 9 regions of the brain, including several in the default mode network, a network involved in introspection that has been implicated in other chronic pain syndromes. Changes in functional connectivity between patients with SCD with and without chronic pain suggest a mechanism for chronic pain that involves neuro-plastic changes to the brain.

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OBJECTIVES: Central poststroke pain (CPSP) is the neuropathic pain in areas of the body corresponding to stroke lesions. It is often refractory to treatment, reduces quality of life, and impedes rehabilitation. The pharmacological treatment of CPSP is challenging. Duloxetine, a serotonin-norepinephrine reuptake inhibitor, is known to be effective against neuropathic pain. The current study describes the efficacy of duloxetine in reducing pain severity in CPSP patients. SUBJECTS AND METHODS: For the purpose of this study, CPSP was defined as spontaneous pain within an area of the body corresponding to the brain lesion that emerged at or after stroke onset. Any previously prescribed medical therapy for the patients was not changed or stopped; duloxetine 30 mg was added to their ongoing treatment. Pain was assessed at baseline and thereafter at 1 and 3 weeks using Numeric Rating Scale (NRS) and Short-form MC Gill Pain Questionnaire scores. At the first follow-up, scores were reviewed and dose was doubled if no improvement or adverse effects were observed. RESULTS: From a total of 37 patients, 4 were withdrawn because of adverse effects including nausea, agitation, and somnolence. The mean elapsed time of observed symptoms since stroke onset was 3.1 ± 4.1 years. There was a significant difference between the mean values of Short-form MC Gill Pain Questionnaire and NRS scores at baseline and those at the follow-up assessment. Twenty-six (70.3%) of the patients showed at least 30% reduction of NRS compared with baseline at the third week. CONCLUSIONS: Our findings suggest that duloxetine can be effective for managing CPSP.

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BACKGROUND: Chronic opiate use leads to a sensitized behavioral response to acute pain, which in turn, leads to escalating doses of opiates. This study was designed to test the hypothesis that chronic opiate usage is also associated with a sensitized neurobiological response to acute pain in individuals that have used prescription opiates for 6 or more months. METHODS: Fourteen patients with non-alcoholic chronic pancreatitis that have been taking prescription opiates for 6 or more months and 14 gender matched, non-opiate using controls were enrolled. Functional neuroimaging data was acquired while participants received blocks of thermal stimulation to their wrist (individually-tailored to their pain threshold). RESULTS: Self-reported pain was significantly greater in opiate using patients (3.4 ± 3.4) than controls (0.2 ± 0.8: Brief Pain Inventory p < 0.005), however no significant difference between groups was observed in the individually-tailored pain thresholds. Opiate using patients evidenced a significantly greater response to pain than controls in two established nodes of the "Pain Matrix": somatosensory cortex (pFWE≤0.001) and anterior cingulate cortex (p ≤ 0.01). This response was positively correlated with prescribed morphine equivalent dosages (average: 133.5 ± 94.8 mg/day). CONCLUSION: The findings suggest that in chronic pancreatitis patients, a dose of opiates that normalizes their behavioral response to acute pain is associated with an amplified neural response to acute pain. Further longitudinal studies are needed to determine if this neural sensitization hastens a behavioral tolerance to opiates or the development of an opioid use disorder.

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BACKGROUND: Spinal cord stimulation (SCS) is a well-established therapy for chronic pain syndromes, with growing applicability to other conditions. Restless legs syndrome (RLS) is a widespread, chronic movement disorder managed primarily and incompletely by medication, and its etiology can be classified as idiopathic or secondary. METHODS: Three patients underwent SCS implantation for chronic back and/or leg pain with concomitant targeting of RLS: (1) a 34-year-old man with sporadic RLS symptoms that strongly intensified after military-related spinal fractures, (2) a 54-year-old man with RLS likely secondary to meralgia paresthetica, and (3) a 42-year-old man with low back and right lower extremity pain after a military motor vehicle accident. RESULTS: Continuing through 40-month, 2-month, and 28-month follow-ups, respectively, the patients experienced exemplary relief of their RLS symptoms. Notably in the case of patient 1, this benefit appears separate from his pain relief, as during the 5-month period directly after surgery but before adjusted targeting, he only experienced pain alleviation. CONCLUSIONS: To our knowledge, this is the first reported case of using SCS as a potentially long-lasting, safe, and highly effective therapy for RLS of mixed etiology. Additionally, 2 patients with RLS possibly secondary to chronic pain also benefited from the therapy. This success may be due to increased inhibition from hypothalamic cells controlling dopaminergic input to the spine.

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OBJECTIVE: To investigate the whole-brain resting-state functional connectivity in patients with chronic migraine (CM) using a data-driven method. METHODS: We prospectively recruited patients with either episodic migraine (EM) or CM aged 18-60 years who visited the headache clinic of the Samsung Medical Center from July 2016 to December 2017. All patients underwent 3 T MRI using an identical scanner. Patients were considered interictal if they did not have a migraine headache at the day and ± 1 days of functional MRI acquisition. Using the group-independent component analysis (ICA), connectivity analysis with a weighted and undirected network model was performed. The between-group differences in degree centrality (DC) values were assessed using 5000 permutation tests corrected with false discovery rate (FDR). RESULTS: A total of 62 patients (44 EM and 18 CM) were enrolled in this study. Among the seven functionally interpretable spatially independent components (ICs) identified, only one IC, interpreted as the pain matrix, showed a significant between-group difference in DC (CM > EM, p = 0.046). This association remained significant after adjustment for age, sex, migraine with aura (MWA), allodynia, depression, and anxiety (p = 0.038). The pain matrix was functionally correlated with the hypothalamus (p = 0.040, EM > CM) and dorsal raphe nucleus (p = 0.039, CM > EM) with different levels of strength in EM and CM. CONCLUSION: CM patients have a stronger connectivity in the pain matrix than do EM patients. Functional alteration of the pain network might play a role in migraine chronification.

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Biomarkers indicating characteristic alterations in the brains of pain patients would in comparison to behavioral examinations allow for earlier diagnoses of pain disease development, a more immediate monitoring of pain disease progression, and for the development of interventions to reverse or compensate for the alterations. To reveal causal relations between an observed alteration and the pain disease longitudinal examinations are essential. Resting-state fMRI examinations can readily be included in large longitudinal cohorts allowing to achieve sufficiently large patient samples even for rare diseases. Our literature review on longitudinal resting-state fMRI examinations of pain patients indicates that pain chronicity is predicted by alterations to the brain's reward system and default mode network. A brain wide reorganization of the resting-state networks is associated with the emergence of the chronic pain state. The functional connectivity of the left frontoparietal network predicts the evolution of pain intensity in the chronic state. Further investigations are necessary concerning the generalization of the biomarkers across the phases in pain development especially for the healthy state, across different pain etiologies, and their specificity to chronic pain. The currently acquired representative longitudinal cohorts will allow for clarification of those issues within the next decades.

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In order to shed light on the first application of human functional stereotactic neurosurgery, whether it was in the realm of movement disorders, as has been claimed repeatedly, or in the realm of psychiatry, a review of the original scholarly literature was conducted. Tracking and scrutinising original publications by Spiegel and Wycis, the pioneers of human stereotactic neurosurgery, it was found that its origin and the very incentive for its development and first clinical use were to avoid the side effects of frontal leucotomy. The first applications of functional stereotactic neurosurgery were in performing dorsomedial thalamotomies in psychiatric patients; it was only later that the stereotactic technique was applied in patients with chronic pain, movement disorders and epilepsy. Spiegel and Wycis' first functional stereotactic operations were for obsessive-compulsive disorder, schizophrenia, and other psychiatric conditions.

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A critical component of brain network architecture is a robust hub structure, wherein hub regions facilitate efficient information integration by occupying highly connected and functionally central roles in the network. Across a wide range of neurological disorders, hub brain regions seem to be disrupted, and the character of this disruption can yield insights into the pathophysiology of these disorders. We applied a brain network-based approach to examine hub topology in fibromyalgia, a chronic pain condition with prominent central nervous system involvement. Resting state functional magnetic resonance imaging data from 40 fibromyalgia patients and 46 healthy volunteers, and a small validation cohort of 11 fibromyalgia patients, were analyzed using graph theoretical techniques to model connections between 264 brain regions. In fibromyalgia, the anterior insulae functioned as hubs and were members of the rich club, a highly interconnected nexus of hubs. In fibromyalgia, rich-club membership varied with the intensity of clinical pain: the posterior insula, primary somatosensory, and motor cortices belonged to the rich club only in patients with the highest pain intensity. Furthermore, the eigenvector centrality (a measure of how connected a region is to other highly connected regions) of the posterior insula positively correlated with clinical pain and mediated the relationship between glutamate + glutamine (assessed by proton magnetic resonance spectroscopy) within this structure and the patient's clinical pain report. Together, these findings reveal altered hub topology in fibromyalgia and demonstrate, for the first time to our knowledge, a neurochemical basis for altered hub strength and its relationship to the perception of pain.

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